The proposed work is a continuation of investigation on the genetic and biochemical basis of methicillin resistance in Staphylococcus aureus. Our prior work has shown that staphylococci become effective transductional recipients for the gene(s) determining methicillin resistance only if they harbor certain prophages and, in most cases, an appropriate penicillinase plasmid. Elimination of the prophage in a methicillin resistant strain eliminates or greatly impairs methicillin resistance. During the coming year we plan to make mutants of prophages and penicillinase plasmids to determine whether specific genetic sites govern their roles in determining recipient-effectiveness for transduction of methicillin resistance.